Lifetime Benefits and Harms of Prostate-Specific Antigen-Based Risk-Stratified Screening for Prostate Cancer.
Lifetime Benefits and Harms of Prostate-Specific Antigen-Based Risk-Stratified Screening for Prostate Cancer.
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DOI:
10.1093/jnci/djaa001
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发表时间:
2020-10-01
期刊:
影响因子:
--
通讯作者:
Etzioni R
中科院分区:
文献类型:
--
作者:
Heijnsdijk EAM;Gulati R;Tsodikov A;Lange JM;Mariotto AB;Vickers AJ;Carlsson SV;Etzioni R
Studies conducted in Swedish populations have shown that men with lowest prostate-specific antigen (PSA) levels at ages 44–50 years and 60 years have very low risk of future distant metastasis or death from prostate cancer. This study investigates benefits and harms of screening strategies stratified by PSA levels. PSA levels and diagnosis patterns from two microsimulation models of prostate cancer progression, detection, and mortality were compared against results of the Malmö Preventive Project, which stored serum and tracked subsequent prostate cancer diagnoses for 25 years. The models predicted the harms (tests and overdiagnoses) and benefits (lives saved and life-years gained) of PSA-stratified screening strategies compared with biennial screening from age 45 years to age 69 years. Compared with biennial screening for ages 45–69 years, lengthening screening intervals for men with PSA less than 1.0 ng/mL at age 45 years led to 46.8–47.0% fewer tests (range between models), 0.9–2.1% fewer overdiagnoses, and 3.1–3.8% fewer lives saved. Stopping screening when PSA was less than 1.0 ng/mL at age 60 years and older led to 12.8–16.0% fewer tests, 5.0–24.0% fewer overdiagnoses, and 5.0–13.1% fewer lives saved. Differences in model results can be partially explained by differences in assumptions about the link between PSA growth and the risk of disease progression. Relative to a biennial screening strategy, PSA-stratified screening strategies investigated in this study substantially reduced the testing burden and modestly reduced overdiagnosis while preserving most lives saved. Further research is needed to clarify the link between PSA growth and disease progression.
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影响因子:
--
作者:
Aus, G;Damber, JE;Hugosson, J
通讯作者:
Hugosson, J
DOI:
10.1136/bmj.c4521
发表时间:
2010-09-14
期刊:
BMJ (Clinical research ed.)
影响因子:
--
作者:
Vickers AJ;Cronin AM;Björk T;Manjer J;Nilsson PM;Dahlin A;Bjartell A;Scardino PT;Ulmert D;Lilja H
通讯作者:
Lilja H
DOI:
10.1056/nejmoa1311593
发表时间:
2014-03-06
期刊:
The New England journal of medicine
影响因子:
--
作者:
Bill-Axelson A;Holmberg L;Garmo H;Rider JR;Taari K;Busch C;Nordling S;Häggman M;Andersson SO;Spångberg A;Andrén O;Palmgren J;Steineck G;Adami HO;Johansson JE
通讯作者:
Johansson JE
影响因子:
39.2
作者:
Gulati R;Gore JL;Etzioni R
通讯作者:
Etzioni R
影响因子:
6.4
作者:
Jonsson, Hakan;Holmstrom, Benny;Stattin, Par
通讯作者:
Stattin, Par